Electromagnetic field stimulator devices, in which a generator of pulsating, variable current is able to feed at least one solenoid for generating an electromagnetic field directed onto a portion of the human body comprising bone tissue, are well known.
For example, American patent U.S. Pat. No. 3,820,534 published in 1974 describes a device able to allow the growth and repair of bone tissue via the electromagnetic field generated by a solenoid powered by an alternating electric signal with a frequency of less than 50 Hz.
Currently known devices are not capable of protecting articular cartilage from degeneration, or rather are not capable of efficaciously operating on the integrity of cartilaginous tissue, activating a preserving effect against the degradation of the cartilage itself.
As is known, the degeneration of articular cartilage manifests itself very frequently and it progressively worsens with age. Suffice it to think that alterations of the cartilage surface only manifest themselves in 5% of the population below 25 years of age, while they are present in more than 80% of people over 75. However, cartilage degeneration is not just a consequence of ageing, but also the end result of a complex series factors related to problems of a biological nature and/or mechanical problems.
Articular cartilage does not possess significant self-healing capabilities other than for small lesions when in youth. The quality and mechanical properties of articular cartilage can only diminish in the course of life.
Of the causes that can damage articular cartilage, we can identify those with a mechanical basis and those with a biological basis
Mechanical causes can be acute or chronic, depending respectively on whether the result of a severe trauma or an alteration of the load axis.
The biological causes are mainly due to the presence of inflammation ascribable to subchondral bone and intraarticular structures (synovial in particular). Inflammatory processes produce a strong catabolic effect on cartilage, because the inflammatory cells synthesize and release pro-inflammatory cytokines (interleukin 1 and 6, and TNF-α) that inhibit the synthesis of proteoglycans by the chondrocites and increase the synthesis of enzymes (matrix metalloproteinase 3, MMP3), which in turn degrade the cartilaginous matrix. The inflammatory response of the articular structures is often the consequence of acute or chronic traumas, distortions, avascular bone necrosis of the subchondral bone, bone marrow edema of the condyles, and side effects of open or arthroscopic surgery.
On the basis of these premises, it becomes fundamental to have a therapy at hand capable of locally controlling the inflammation, at both the subchondral bone and articular structure levels. The therapy must also be able to act directly on the chondrocites in the depth of the cartilage to prevent the catabolic effects of the inflammatory cytokines on the chondrocite and on the matrix, to facilitate anabolic activities and the synthesis of proteoglycans. The simultaneous treatment of cartilage, subchondral bone tissue and articular fleshy structures is only practicable with physical means.
Based on this premise, the need is thus felt for realizing a device that is capable of putting that specified above into effect.